A new scientific mystery and a potential new Omicron-like event

We have a new scientific mystery and we’ll find out the implications this autumn.

The new version of SARS2 spreading around the globe is called EG.5.1. Normally, when a new version of this virus spreads, it does so because it changed its Spike protein sufficiently to make the antibodies useless (immune evasion).

But then came XBB. And as I mentioned before, what you see with XBB is that an infection doesn’t induce neutralizing antibodies against it, in mice who have already been infected by the original strain.

And now we have a new study from Japan that looks at this, confirming this strange problem:

As of July 2023, EG.5.1 (a.k.a. XBB., a XBB subvariant bearing the S:Q52H and S:F456L substitutions, alongside the S:F486P substitution (Figure S1A), has rapidly spread in some countries. On July 19, 2023, the WHO classified EG.5 as a variant under monitoring. First, we showed that EG.5.1 exhibits a higher effective reproduction number compared with XBB.1.5, XBB.1.16, and its parental lineage (XBB.1.9.2), suggesting that EG.5.1 will spread globally and outcompete these XBB subvariants in the near future. We then addressed whether EG.5.1 evades from the antiviral effect of the humoral immunity induced by breakthrough infection (BTI) of XBB subvariants and performed a neutralization assay using XBB BTI sera. However, the 50% neutralization titer (NT50) of XBB BTI sera against EG.5.1 was comparable to those against XBB.1.5/1.9.2 and XBB.1.16. Moreover, the sensitivity of EG.5.1 to convalescent sera of XBB.1- and XBB.1.5-infected hamsters was similar to those of XBB.1.5/1.9 and XBB.1.16. These results suggest that the increased Re of EG.5.1 is attributed to neither increased infectivity nor immune evasion from XBB BTI, and the emergence and spread of EG.5 is driven by the other pressures. We previously demonstrated that Omicron BTI cannot efficiently induce antiviral humoral immunity against the variant infected. In fact, the NT50s of the BTI sera of Omicron BA.1, BA.2, and BA.5 against the variant infected were 3.0-, 2.2-, and 3.4-fold lower than that against the ancestral B.1.1 variant, respectively. However, strikingly, we found that the NT50 of the BTI sera of XBB1.5/1.9 and XBB.1.16 against the variant infected were 8.7- and 8.3-fold lower than that against the B.1.1 variant. These results suggest that XBB BTI cannot efficiently induce antiviral humoral immunity against XBB subvariants.

In other words, you see that the antibodies from the XBB variants are as good at stopping those variants, as they are at stopping EG.5.1. That’s not what normally happens. A new variant normally emerges because it changed its Spike protein enough to make the most potent antibodies most people deploy useless.

But now we’ve run into a situation where this apparently isn’t necessary anymore. Which raises the big question:

So, if this version isn’t better at dodging the antibodies, what is it better at that apparently allows it to rapidly replace its XBB ancestors?

Well, it turns out this new variant looks an awful lot like the Delta variant:

The reason Delta ever took over had less to do with antibody evasion and more to do with the fact that it rapidly produced a lot of copies of itself. This meant that if people’s antibody concentrations were low enough (ie many elderly a few months after vaccination), the virus would spread through their body before concentrations could rise enough to suppress the viral load. It’s only with Omicron, when the Spike in the vaccines became truly mismatched.

But I think there’s another issue we’re dealing with, which would also explain why the virus suddenly seemed to fade away months ago across the world and is now rapidly returning, without having substantially changed its Spike protein: Improved interferon suppression.

If antibodies are high, the virus can’t infect a person. And because people now have antibodies against just about every viral protein and a wide variety of variants, it’s not easy to mutate around that.

And so rather than mutating to avoid antibodies, another strategy for survival would be to wait until the antibodies fade and then to infect people in a manner that prevents the infected cells from sending a warning signal that they have been infected. That’s the route that EG.5.1* seems to represent.

And yet, the other route can not be ruled out. It’s also perfectly possible for a new version of SARS2 to emerge that is once again so different from the recently circulating varieties that the antibody response proves to be useless again. That would be an Omicron-like event. It seems that yesterday, such a discovery may have been made.

In a context where everyone has antibodies against this virus and we constantly try to raise antibodies, any such saltation that emerges, like this saltation discovered yesterday with at least 30 amino acid mutations in Spike, will have a huge selective advantage, regardless of its own intrinsic transmissibility.

And the worst case scenario you may be faced with as a result, is a Dengue-like serotypes scenario. I did not invent this myself, it was warned about here, as well as by a number of other articles.

What happens in a serotypes scenario, is that you end up with multiple very distinct looking SARS2 viruses circulating simultaneously. But importantly, antibodies against Serotype 1 induced by an infection, would cause antibody dependent enhancement for Serotype 2 and vice versa. And because these Serotypes depend on each other, they would continue to circulate simultaneously.

Such serotypes could emerge pretty much instantaneously, from persistent infections, or spillovers from animal populations. If the new variant discovered yesterday proves fit enough to spread through the population (still uncertain), it may reveal itself to be such a serotype strain: One that does not replace the XBB family but co-exists besides it, both feeding off each other.

The reality is that antibodies against Spike, are just not a sustainable way for our immune systems to deal with the circulation of the virus. Only about 10% of the population is infected by influenza in a typical year, so you don’t have to worry too much about antibody mismatches.

But with SARS-COV-2, we see that the average person is infected at least twice a year, by rapidly evolving variants. In such a scenario, antibodies against the Spike protein are not going to solve the problem for us. By training people’s immune systems to induce a strong IgG antibody response against the Spike protein, we merely made the pandemic worse: We taught the immune system to bring the wrong weapon to the battle.

For viruses like this, the innate immune system has to do the job.


  1. Our whole family is never-tested, never-jabbed purebloods. Never isolated ourselves, traveled, and wore masks as little as possible back when they were mandated.

    We got whatever variant has been circulating around here (USofA) these last few weeks. Mild enough to not even warrant taking the day off. Symptoms are different than the strains we have been getting since Omicron (which were more on the “neuro” side, and less on the respiratory/digestive side), and they resemble more what we got in 2020. Symptoms vary somewhat from person to person. The most different thing by all variants so far is that the kids seem more affected by it than the adults. One of them even got shortness of breath / weight on the chest. Just reporting this as an anecdotical data point.

    Unrelated: I came across a study y’all may find useful. Maybe it applies more to the Omicron variants than the current one: https://www.zerohedge.com/political/covid-19-vagus-nerve-inflammation-may-lead-dysautonomia-new-study

    Thanks for keeping a finger on the pulse of this interesting problem. Hard to find today a place where things are discussed cooly, without an agenda (“covids will kill us all, hence give up your freedoms and get the clotshots!” vs the counter-reaction “virus is nothing or doesn’t exist, we are all 100% fine!”). Places that already have a large audience, like Igor’s substack, likely have to mind what they say lest they should unwittingly provide a reason for the vaxxists / weffers to start a new offensive.

  2. >Symptoms vary somewhat from person to person. The most different thing by all variants so far is that the kids seem more affected by it than the adults. One of them even got shortness of breath / weight on the chest.

    Yeah this is exactly what you would expect in response to improved interferon antagonism. It also fits what we see in the hospitalization numbers: Mostly children getting hospitalized now.

    • The “real deal” pandemics seem to come in waves that take years to play out. The main event of the Black Death in Europe was 1346-1353 (seven years), followed by other waves in 1360–63; 1374; 1400; 1438–39; 1456–57; 1464–66; 1481–85; 1500–03; 1518–31; 1544–48; 1563–66; 1573–88; 1596–99; 1602–11; 1623–40; 1644–54; and 1664–67 (sources at https://en.wikipedia.org/wiki/Black_Death#Second_plague_pandemic ). The natural selection event you discuss at https://www.rintrah.nl/an-old-enemy-left-his-scars-in-your-genetic-code/ also may have played over several generations, as unfit progeny that emerged was wiped out repeatedly. We are already in our fourth year of coronafun. Maybe this will take decades to play out.

      • Yeah that’s true.

        But also consider smallpox: It was a mild childhood illness throughout the medieval era. And then for whatever reason, it evolved into a very virulent virus that killed about a quarter of people it infected. We don’t know why.

        There’s just no obvious law that requires a virus like this to evolve to become less virulent.

        And we don’t really have a way to get rid of this virus either. It persistently infects millions of people worldwide, it has already established animal reservoirs and it can infect our own pets.

        The best scenario I can think of is when our own immune system gradually selects less virulent variants. That’s what the NK cells seem able to do, they do it with Influenza.

        All these attempts to reduce transmission of SARS-COV-2 through improved ventilation etcetera sound nice in theory, but you’re not just stopping SARS-COV-2 from spreading, but all other respiratory viruses too. If immunity against those other viruses wanes, it results in all sorts of potential risks.

        There’s probably some law of immunology that forces the hCovs to be mild. NK cells aggressively selecting against cytopathic varieties would be a candidate for such a mechanism.

        The problem of course is that when you vaccinate everyone, you’re inducing an antibody response, rather than an NK cell response. And I don’t see how our antibody response could select against virulence. In fact, I’d say it does the opposite (by encouraging interferon antagonism).

  3. “antibodies against Serotype 1 induced by an infection, would cause antibody dependent enhancement for Serotype 2 and vice versa.”

    If such a nightmare scenario manifests itself over the coming months, would the presence of trained innate cellular immunity and specifically the NK cells residing in the organs and tissues of the unvaccinated protect them from serious disease (ADE)?

    • I wonder that too. This stuff isn’t really properly being studied unfortunately.

      We know that the NK cells are very important in reducing influenza infection severity. Evidence suggests they seem to have an important role in SARS-COV-2 too.

      I haven’t seen any studies in regards to how vaccinated and unvaccinated people differ in their NK cell population.

      I expect that innate immunity has been largely sidelined, with antibodies against Spike induced by mRNA vaccination, especially before any infection, preventing NK cells from receiving the training they need.

      mRNA vaccination is known to cause immune system reprogramming that even shows up for other pathogens. The NK cell response to other pathogens may also have been affected. It’s far more reckless than the Adenovirus vector vaccines, which at least resemble a viral infection.

      We would know what the situation is, if it would be studied. But this would require autopsy studies, you can’t just study people’s blood for this, so it doesn’t seem likely to be studied anytime soon.

      NK cells have receptors to which the Spike protein has to bind regardless of its mutations, because they resemble the receptors viruses use to enter cells. NK cells would thus be expected to be able to do their job, regardless of serotypes.

      However, most unvaccinated people still show an IgG antibody response against SARS2. So ADE from serotypes would be a concern for them too.

      • Would outdoor exercise in both heat and cold, which is known to strengthen the body in general, help improve innate immunity / NK cells? What other lifestyle factors can help? Sleep? Reducing stress?

        • The best evidence I’ve seen for improving the NK cell response against SARS2 is… catching malaria. But I can’t really recommend that to anyone.

          In general, the best advice to offer anyone is just to maintain a generally healthy lifestyle and not to worry too much. Saunas, natto and Endurance exercise are things that we know are important to maintain healthy blood vessels.

          Cannabis is good at removing the beta amyloid that builds up in people’s brains and leads to Alzheimer’s, nicotine seems to be good at removing the alpha synuclein that builds up resulting in parkinson’s. Finally, psilocybe mushrooms seem good at healing the blood vessels too.

          Almost all the stuff you can do against SARS2, is stuff you should be doing already anyway.

  4. Thanks for the update, I am no longer on Twitter so I don’t regularly consume all the latest news from the variant trackers anymore. You and Geert hace clearly laid out the evolutionary checkpoints the virus will likely undergo, and we have already passed plenty of them. So the trend is very clear for everyone who is looking.
    I am just waiting for the effects to show in daily life. We’ll get there at some point I guess.

    • The new variant _can_ cause more hospitalizations and deaths, but will it? The proof is in the pudding. Know a tree by its fruit. Make pudding with the fruit.

      • The covid pudding may take some time to thicken. By some time, I mean in terms of human psychology; we are built to discount threats that take a while to emerge. In the case of AIDS, your first symptoms are like a mild cold. Then the virus takes up residence for ten years in hidden spots like your microglia, eating away at your immune system. Then your immune system finally gives out and you end up dying of some awful opportunistic disease. If you read the studies that Daniel Brittain Dugger links, it sure looks like that is what is going to happen with covid, but faster. DBD is not a genius and he is somewhat repetitive, but he’s probably right. He’s willing to face this, as most people aren’t, since he’s already on ongoing treatment for HIV infection, so he can see a world in which everyone needs ongoing antivirals for covid infections that can’t be truly cleared. Since people are already getting stupider and stupider due to the cognitive effects of covid infection that may lessen the suffering.

        • I am not yet ready to fully buy that Covid is AIDS but airborne. The main reason for my doubt is that no old Covid lineages are shed and reappearing like they would if the virus was active in body tissues.

          I am VERY open to such a possibility as I suspect grand malfeasance, however I have not yet seen convincing evidence of such HIV-like activity, yet.

          • There’s a lot of talk about how covid mutates in the immunosuppressed. We get to hear about how someone who had it in their system for 300 days produced some very different strain (which typically isn’t suited for spread). But the virus also mutates in regular people who have it. It mutates like crazy. So people wouldn’t necessarily be hosting and spreading the strain they caught; they might have caught Wuhan but they are breeding something else.

            Also, to the extent that they caught and still have the same strain, everyone around them was already exposed to that strain so it’s not going to become a big outbreak again; there is immunity to that particular strain. Even if someone is still harboring Wuhan, hardly anyone around them is going to catch it from them due to prior exposure.

            Also, I have read that strains drive out other strains (like covid driving out the flu early on, for instance); couldn’t it be that someone is sitting around still full of Wuhan, but it doesn’t spread from them due to being driven out by other strains?

            They’re finding the virus in every body system in cadavers of people who were sick for a very long time. So it is sticking around in the body. It is possible that it is sticking around in a person, without being transmittable to another person. It was a respiratory virus, but now it is in the brain (for instance), which is a part of the body which is protected from the immune system. And so it could be permanent like HIV, but not spreading to the surrounding population. It sits in the brain, held in check by the immune system, until the immune system ultimate fails and it gets out again (like with HIV).

            The real reason I think this is that I just don’t know why a person WOULD clear it. I mean, it causes syncytia. Including in the brain. It causes cells to fuse together and then several cells are just one big cell with a jumble of cell contents. How would the body fix that? It doesn’t. Do syncytial cells produce more virus? Actually I’m not sure.

            Sorry this is rambling and in parts self-contradictory; my last biology class was in my first year of college in 1981, but I know how I am betting. Government-funded morons playing around.

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The patients in the mental ward have had their daily dose of xanax and calmed down it seems, so most of your comments should be automatically posted again. Try not to annoy me with your low IQ low status white male theories about the Nazi gas chambers being fake or CO2 being harmless plant food and we can all get along. Have fun!

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